Improved myocardial efficiency in the working perfused heart of the spontaneously hypertensive rat.

Tubau, Julio F.; Wikman‐Coffelt, Joan; Massie, Barry M.; Sievers, Richard E.; Parmley, William W.

doi:10.1161/01.hyp.10.4.396

Cited by 25 publications

(12 citation statements)

References 31 publications

(16 reference statements)

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“…Similarly, in the rat after a short-or long-term pressure overload caused by abdominal aortic stenosis, myocardial mechanical efficiency remained unchanged [26]. However, oxygen consumption studies on hearts obtained from 6-month-old spontaneously hypertensive rats did reveal a higher mechanical efficiency than that of age-matched Wistar-Kyoto control rat hearts [27]. It is important to realize that in whole heart studies, the efficiency measure usually incorporates the basal oxygen consumption in the denominator and hence an increase in the mechanical efficiency may, in fact, be due to a decrease in the energetic cost of the basal metabolism.…”

Section: Energeticsmentioning

confidence: 94%

Mechanical and energetic changes in short-term volume and pressure overload of rabbit heart

et al. 1992

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The mechanical and energetic consequences of a short-term volume overload (STVOL) hypertrophy and short-term pressure overload (STPOL) hypertrophy have been investigated in rabbits and compared with short-term sham-operated controls (STSOC). Hypertrophy was induced either by creating an aortocaval shunt (volume overload) or by banding the pulmonary artery (pressure overload). Suitable papillary muscles were excised from the hearts 8-10 days after the surgical procedure. At 27 degrees C and a stimulus frequency of 1.0 Hz, peak stress development of the STVOL preparations was significantly reduced from the control group, whereas no significant difference in peak stress development was evident between the STPOL and STSOC groups. Surprisingly, the STPOL preparations displayed pulsus alternans after only 8-10 days of inducing the overload. At steady-state conditions, the isometric 10%-90% rise times, the 90%-10% relaxation times, and the 1/2-widths were not significantly different between the treated and control groups. In isotonically contracting muscles working against a range of afterloads, the enthalpy (energy) and work output of the STVOL and STPOL preparations were depressed compared to the STSOC preparations; the differences were statistically significant for the STVOL group. Due to the parallel change in work and enthalpy, the mechanical efficiency was unaltered. A force-length-area (FLA) analysis, analogue of the pressure-volume-area (PVA) analysis, was applied to the isotonic data of this study. The isotonic enthalpy at the various load levels was plotted against the measured FLA and the data were fitted by linear regression. It was evident that the FLA correlated closely with the energy used. The STVOL and STPOL mean total energy:FLA regression lines lay parallel to but were below the STSOC line, signifying a drop in the activation heat, although this reduction did not achieve statistical significance. It is concluded that significant mechanical and energetic changes are evident after a short-term volume overload although earlier work has shown that these differences are absent at the later, compensated stage of hypertrophy. Changes associated with the pressure overload model suggest a disturbance in calcium regulation: this effect is also seen in long-term pressure overload.

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Section: Energeticsmentioning

confidence: 94%

Mechanical and energetic changes in short-term volume and pressure overload of rabbit heart

et al. 1992

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“…17,18 Previous studies have demonstrated that there is a normal energy metabolism in hearts of young SHR (12-25 weeks). 14,19 On the other hand, only very few data exist concerning the myocardial energy metabolism of aged SHR (Ͼ40 weeks) suffering from progressive myocardial dysfunction. Carlier et al 11 found reduced PCr in the isolated hearts of 72-week-old SHR, and Mochizuki et al 10 in the hearts of 44-week-old SHR after an ischemic period compared with control hearts.…”

Section: Age-dependent Alterations Of Myocardial Performance and Enermentioning

confidence: 99%

Age-related decline of PCr/ATP-ratio in progressively hypertrophied hearts of spontaneously hypertensive rats

et al. 2000

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Although the ultimate cause for the myocardial dysfunction of hypertensive heart disease is still unclear, a crucial role of the myocardial energy metabolism has been suggested. Therefore, the aim of the present study was to investigate whether age-related myocardial dysfunction in hearts of spontaneously hypertensive rats (SHR) is associated with an impaired myocardial energy metabolism. Isolated hearts of SHR and Wistar Kyoto rats (WKY) aged about 40, 60, and 80 weeks, respectively (each n = 4-5), were perfused according to the working heart technique. Cardiac work and coronary flow were monitored online. Myocardial energy metabolism was evaluated by calculating the ratio of phosphocreatine (PCr) and adenosine triphosphate (ATP) which were measured by nuclear magnetic resonance (31P-NMR) spectroscopy. All hearts were subjected to work for 30min at baseline conditions (low afterload), followed by another 30min under a moderate pressure load (high afterload). Each SHR group showed a higher heart weight/body weight ratio than the age-matched WKY controls. The SHR showed a progressive age-dependent reduction of cardiac work (40 weeks = 5.1+/-0.3, 60 weeks = 4.0+/-0.3, 80 weeks = 3.8+/-0.2 (mW/g) at baseline conditions) and PCr/ATP-ratio (40 weeks = 1.82+/-0.06, 60 weeks = 1.69+/-0.05, 80 weeks = 1.59+/-0.09 (PCr/ATP) at baseline conditions). Similar results were found for hearts of SHR at high afterload. In WKY no significant decline in cardiac work or PCr/ATP-ratio was found under either low or under high afterload. The cardiac work capacity of hearts of SHR progressively decreases with increasing age and left ventricular hypertrophy. This myocardial dysfunction is closely associated with an impaired PCr/ATP-ratio, suggesting a decreased energy reserve.

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“…31p-NMR data are shown for healthy and myopathic hamster hearts. The sugar phosphates were identified as described by Chance et al (29). The intracellular pH was calculated as described in methods.…”

Section: Resultsmentioning

confidence: 99%

Glycolysis in heart failure: a31P-NMR and surface fluorometry study

Auffermann

Parmley

et al. 1990

Basic Res Cardiol

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Glycolysis is slow in the heart, especially in the cardiomyopathic heart. Glycolysis is partially rate-limited by phosphofructokinase (PFK), an enzyme which is inhibited by calcium (Ca2+)i and hydrogen ions (H+)i and activated by cAMP. (H+)i and (Ca2+)i are augmented in cardiomyopathy. With glucose as the only substrate (NADH)/(NAD) the phosphorylation potential and developed pressure were significantly lower, and concentrations of phosphomonoester sugars and hydrogen ions (H+)i were significantly higher in isolated cardiomyopathic hearts as compared to healthy hamster hearts. Pyruvate lowered diastolic (Ca2+)i in cardiomyopathic hamster hearts. With pyruvate as the substrate (NADH)/(NAD), the phosphorylation potential and developed pressure increased significantly and concentrations of phosphomonoester sugars (PME), (H+)i and diastolic (Ca2+)i decreased significantly in myopathic hamster hearts. The results suggest that late heart failure in the myopathic hamster is associated with calcium and/or hydrogen ion-induced inhibition of glycolysis.

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Improved myocardial efficiency in the working perfused heart of the spontaneously hypertensive rat.

Cited by 25 publications

References 31 publications

Mechanical and energetic changes in short-term volume and pressure overload of rabbit heart

Mechanical and energetic changes in short-term volume and pressure overload of rabbit heart

Age-related decline of PCr/ATP-ratio in progressively hypertrophied hearts of spontaneously hypertensive rats

Glycolysis in heart failure: a31P-NMR and surface fluorometry study

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